After the publication of this article [1], concerns were raised about identical tables across distinct time points and contradictory statements. Here, the authors have provided additional information to clarify these issues:

In the Results section of this paper, Tables 1 and 2 contain duplicate data as that of Table 4 by error. Tables 1–5 -5 are intended as summaries of the data presented in S3 Table, which are correct. Please see the corrected Tables 1 and 2 here.

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Table 1. Top DEGs in bovine endometrium at 12 h post-CIDR removal versus oestrus, ranked by ascending B-H FDR.

https://doi.org/10.1371/journal.pone.0324686.t001

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Table 2. Top DEGs in bovine endometrium at 24 h post-CIDR removal versus oestrus, ranked by ascending B-H FDR.

https://doi.org/10.1371/journal.pone.0324686.t002

The authors have provided the following corrections

In the Discussion section, the fourth paragraph under the subheading “Tissue remodelling and innervation in the proliferative phase” is incorrect. This paragraph should be disregarded.

In the Discussion section, the statement comprising the fourth and fifth sentences in the seventh paragraph under the subheading “Tissue remodelling and innervation in the proliferative phase” is incorrect. These sentences should be disregarded. The corrected paragraph is:

“For both time points before oestrus, transforming growth factor beta 1 (TGF-β1), the cytokine tumour necrosis factor (TNF), and HDAC (group of histone deacetylases) were among the top ranked upstream regulators (Table 7). TGF-β1 is required for the development of smooth muscle in the female reproductive tract [93], as well as being present in seminal fluid and altering the endometrium and oviduct to promote embryonic development and implantation [94]. In humans, expression of TNF has also been shown to rise in the mid- to late-proliferative phases [95], while in bovine endometrial cells, TNF-induced production of chemokines [96], directs the migration of leukocytes to inflammation sites [97]. These observations suggest that endometrial immunity is upregulated at this timepoint, actively preparing for sperm deposition and pathogen entry. The top interaction networks for CIDR+12 h and CIDR+24 h are centred on the transcription factor NFκB complex (Figs 4 and 5) although these are different networks. For the CIDR+12 h top network, involved in Endocrine system disorders, Hereditary disorders and Organismal injury and abnormalities, NF-κB is linked to various hub genes, such as SUSD4, which negatively regulates complement activation, and ALDH1B1, which links to various aldehyde dehydrogenases. The top network for CIDR+24 h is Neurological disease, Nervous System Development and Function and Behavior, with links to voltage-dependent Na+ channels and SYN genes, encoding synapsins that are associated with the trafficking of synaptic vesicles.”